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7.2 Hypoglycemia; Jaundice

Pathologic Neonatal Hypoglycemia

Physiology

The term hypoglycemia refers to low blood glucose concentration. The body, and particularly the brain, requires a source of energy to function. Glucose is an important source of energy.

There are two times of crisis in the neonates life regarding energy (glucose) needs. Both crises are managed by normal metabolic adaptation which provides alternative fuel sources for the neonate.
  1. The first crisis occurs when the cord is cut and the maternal supply of glucose to the newborn is abruptly discontinued.1,2
    • blood glucose concentration reaches its nadir in the first 1 - 2 hours
    • blood glucose concentration then rises to a steady state within 2 - 3 hours
    • feeding the infant may cause small transient rises in blood glucose concentration, but it is not feeding that maintains euglycemia
  2. The second crisis will occur if lactation is delayed.3,4,5
    • Fat breakdown occurs, releasing ketone bodies that provide glucose-sparing fuel to the neonatal brain, protecting neurologic function.
Transient hypoglycemia in the early neonatal period is a common adaptive phenomenon as the newborn changes from the fetal state of continuous transplacental glucose consumption to intermittent nutrient supply following cessation of maternal nutrition at birth.
Research has demonstrated that in the term, healthy newborn, this dynamic process is self-limiting and is not considered pathologic.6

Do not screen normal, full term neonates.


Clinically significant (ie pathologic) hypoglycemia does NOT occur in well, full term babies. The baby's physiology protects him against this by using metabolic processes to maintain steady-state glucose concentration. 2

Unnecessary routine screening results in the misidentification of neonates captured while experiencing the normal, self-correcting physiologic blood glucose nadir, who are then diagnosed with pathologic neonatal hypoglycemia.
Subsequent to this misdiagnosis, further surveillance and unnecessary, aggressive treatment interventions will follow that are potentially harmful to the successful establishment of positive maternal-infant interactions and the breastfeeding experience.

Research studies indicate that routine hypoglycemia screens, treatments, and interventions in the healthy infant are not evidence-based and result in a serious disruption of the initiation process and duration patterns of lactation.6

Diagnosing pathologic neonatal hypoglycemia

Prolonged hypoglycaemia, sufficiently severe to cause neurological signs, is called pathologic neonatal hypoglycemia.
Diagnosis is made when
  • neurological signs are present, and
  • blood glucose concentration is low.7

Clinical signs to observe for:

The first observation to make, and the most important, is the infant's level of consciousness. Pick up the infant, talk to him, wake him up. A limp infant you cannot wake is a bad sign.

Other clinical manifestations

  • irritability, tremors, jitters
  • exaggerated Moro reflex
  • high-pitched cry
  • lethargy, limpness, hypotonia
  • apnea or irregular breathing
  • cyanosis
  • hypothermia, temperature instability
  • poor or inadequate sucking reflex
  • vasomotor instability
  • seizures

Which infants are at risk?

Think about which infant's may have metabolic stressor's or immaturity that could affect the normal release of glucose in the first hours following birth, or ketone body metabolism later.

Infants at risk of symptomatic hypoglycemia include:8
  1. Infants of diabetic mothers - hyperinsulinemia as a result of poor maternal control during pregnancy will cause hypoglycemia until stabilised.
  2. Infants who are preterm or late preterm with metabolic immaturity.
  3. Infants who have few fat reserves, eg small for gestational age infants
Infants in these categories require frequent observation for neurological signs and blood screening for glucose concentration at intervals according to evidence-based medical policies.

Workbook Activity 7.3

Complete Activity 7.3 in your workbook.

Preventing pathologic hypoglycemia

Placing ALL newborns in skin-to-skin care with their mother from immediately after birth, and for as long as possible, preferably at least the first day of life, will:
  • stabilise the infant's temperature (no requirement to burn fat for heat)
  • stabilise the infant's cardio-respiratory system
  • stimulate metabolic adaptation
  • initiate the first phase of the enteric nervous system (facilitating intestinal function)
  • reduce stress (release of cortisol initially causes a surge in blood glucose concentration, then a fall)
  • facilitate early and frequent breastfeeding, preventing a delay in lactation
  • and prevent other factors, such as nosocomial infections and hypothermia that cause hypoglycemia.

This is really important!

It's worthwhile repeating: The BEST way for you to prevent hypoglycaemia in the infants you care for is by placing baby in skin-to-skin contact with his mother immediately after birth, and for as long as possible.

Share your thoughts in the forum about how this simple, no-cost practice helps prevent hypoglycemia.

What about early feeding?

Facilitation of early and frequent breastfeeding is strongly encouraged. However, sources of exogenous glucose, such as from colostrum, are not essential to maintain normal glucose concentration in the first 24 hours.

Healthy, full-term infants do not develop symptomatic hypoglycemia in the first 24 hours simply as a result of underfeeding.9

Frequent, effective breastfeeding will, however, be protective after the first 24 hours. Beginning breastfeeding soon after birthing will ensure the infant is breastfeeding well and maternal lactation is becoming established by the time the infant is dependent on this source of energy.

Workbook Activity 7.4

Complete Activity 7.4 in your workbook.

Clinical management of pathologic hypoglycaemia

Inadequately treated symptomatic hypoglycemia has such a serious outcome that pediatricians agree that
the clinician should not rely on oral feeding (eg breastmilk or infant formula) for the correction of symptomatic hypoglycemia 9 and “ symptomatic hypoglycemia should always be treated with a continuous infusion of parenteral dextrose. 8

However, during this medical management, breastfeeding should continue uninterrupted. The goal is to have an infant who suckles effectively at the breast and a mother's milk supply that is able to meet his needs when IV therapy is discontinued.

  • continue breastfeeding, and skin-to-skin contact during treatment
  • do not give water, glucose water or formula to the breastfed infant
  • continue breastfeeding while weaning baby from IV glucose, monitoring carefully

Extend your knowledge

Go to the PDFAcademy of Breastfeeding Medicine and read this protocol on Hypoglycemia. File it in your workbook.

Unit Activity

Access your Unit policy on the management of hypoglycemia. Compare it to the literature published in peer-reviewed journals. Is it up-to-date and evidence-based? If not, form a working group to review it, present it at a Unit meeting and implement it.

What should I remember?

  • How euglycemia is maintained, regardless of oral intake.
  • The effect of unnecessary blood glucose monitoring on the full-term infant.
  • The infants who are 'at-risk' of pathologic neonatal hypoglycemia.
  • How to recognise signs of pathologic hypoglycemia.
  • The best practice management to prevent symptomatic hypoglycemia for all infants.
  • How to support breastfeeding during medical management of pathologic hypoglycemia.

Self-test quiz

Jaundice

The most common paediatric condition encountered in the first week is hyperbilirubinaemia. It is so common that it is termed "Physiological Jaundice" and reflects the normal physiological changes that occur as the neonate adapts to extrauterine life.

Normal serum bilirubin levels

The neonate is more susceptible to high serum bilirubin levels because

  1. there is increased breakdown of fetal erythrocytes. This is the result of the shortened lifespan of fetal erythrocytes and the greater number of erythrocytes in neonates.
  2. liver excretory ability is low because of the relative immaturity of the liver.

At birth neonates have a low serum bilirubin. The normal pattern is for a rise to a peak by the third day of life, followed by a plateau and drop in levels, or, for ⅔ of babies, a gradual rise to another peak on about the 10th day. After this the levels gradually drop until about the third week of life. (An exception to this is found in babies of Asian origin whose Day 3 levels peak nearly twice as high as found in non-Asian babies).

In some mothers, unidentified factors present in her breastmilk may contribute to increased enterohepatic circulation of bilirubin with harmless jaundice persisting for many weeks. This is an extension of physiologic jaundice known as breastmilk jaundice. No special treatment is required and continued breastfeeding is recommended.10



Diagram © Health e-Learning

An explanation of why newborns have elevated bilirubin levels could be that the antioxidant effects of bilirubin compensate for the relative deficiency of endogenous antioxidants in newborns. It is another protective effect denied the artificially fed infant.

Causes of abnormal bilirubin levels

  • Abnormal weight loss : A weight loss of more than 7% in both artificially fed and breastfed infants is associated with higher serum bilirubin concentrations. Inadequate intake causes
    • retention of meconium and reabsorption of previously excreted bilirubin back into the blood stream.
    The cycle is then likely to continue as raised serum bilirubin causes sleepiness and poor feeding, decreased intake and further reabsorption of bilirubin.

  • Hemolytic processes : Blood group incompatibilities (Rh, ABO, and others) may increase bilirubin production through increased haemolysis. Nonimmune haemolytic disorders (spherocytosis, G-6-PD deficiency) also may cause increased jaundice through increased haemolysis.

  • Non-hemolytic processes : A number of other nonhaemolytic processes can increase serum bilirubin levels. Accumulation of blood in extravascular compartments (cephalhaematomas, bruising, occult bleeding) may increase bilirubin production as the blood is absorbed and degraded. Increased bilirubin production also is seen in infants with polycythemia and in infants of mothers with diabetes. Increased reabsorption of bilirubin from the bowel leading to elevated bilirubin levels is seen in infants with bowel obstruction or ileus.

Physical appearance

Jaundice has a cephalocaudal (or cephalopedal) ie head to toe progression; it is evident first in the face, gradually becoming visible on the trunk. Jaundice seen below the level of the umbilicus and on the extremities reflects increasingly higher serum bilirubin levels. Jaundice disappears in the opposite direction.
Daylight on a clear day provides the best lighting for evaluation. Pressure applied on the skin using the finger pad will blanch the skin revealing the underlying colour.

Non-invasive transcutaneous measurement of bilirubin is a reliable screening method for identifying infants who need additional work-up.11 Laboratory measurement of bilirubin is indicated if jaundice involves the lower body and extremities.10

Management of hyperbilirubinemia

Prevention of hyperbilirubinemia due to inadequate intake involves early recognition of risk factors, good teaching and supervision of breastfeeding, and mothers who are able to recognize that good transfer of breastmilk to the infant is occurring.

Low serum bilirubin concentrations in the first 5 days are characterised by optimal breastfeeding behaviours: 10

  • initiation of breastfeeding in the first hour after birth
  • continuous rooming-in with unlimited access to the breast
  • a breastfeeding frequency of 10 to 12 times per day
  • prompt responses to early hunger cues, and
  • absence of all supplementation.

Ensure adequate intake for the infant:

  • assess breastfeeding effectiveness
  • stimulate and support an adequate milk supply
  • frequent breastfeeds; 8-12 per 24 hrs
  • offer supplemental feeds of expressed breastmilk
  • artificial infant formula is given only in the absence of adequate breastmilk volumes
Phototherapy treatment may be required to heighten elimination of bilirubin. If the infant is under phototherapy lights:
  • continue all of the above
  • offer emotional support to the mother while her baby is receiving treatment
  • Contraindicated: water supplementation

Workbook Activity 7.5

Complete Activity 7.5 in your workbook.

Extend your knowledge

Read and print the ExternalAAP Clinical Practice Guidelines for the management of hyperbilirubinemia. Note the recommendations regarding breastfeeding and supplements.

Note that the first two recommendations are to:

  1. promote and support successful breastfeeding, and
  2. harm is associated with supplementing breastfed infants with water or dextrose water.

Unit activity

What is your Unit's policy on recognition, prevention and management of jaundice? Discuss the Unit policy with your colleagues, comparing it to the AAP recommendations and other evidence-based articles. Would the algorithm in the AAP guidelines be useful to reproduce for your Unit?

What should I remember?

  • Jaundice is a normal physiological process in the well full-term baby (physiological jaundice)
  • The potential risk factors for problematic jaundice
  • The optimal management that prevents an abnormal pattern of jaundice

Self-test quiz

Click and drag the missing words below into their correct place

The missing words are: breastfeeding breastmilk physiological supplementation tenth third

__________ jaundice is normal in most newborns. Bilirubin rises to a peak on the __________ day of life, followed by a further rise until the __________ day for most breastfed infants. A harmless form of jaundice that persists for many weeks is termed __________ jaundice.
Prevention of hyperbilirubinemia is focused on frequent, effective __________ and the absence of all __________.

Notes

  1. # Hawdon JM (2010) Best practice guidelines: Neonatal hypoglycaemia.
  2. # Cornblath M et al. (2000) Controversies regarding definition of neonatal hypoglycemia: suggested operational thresholds
  3. # Hawdon JM et al. (1992) Patterns of metabolic adaptation for preterm and term infants in the first neonatal week.
  4. # Edmond J et al. (1985) Ketone body metabolism in the neonate: development and the effect of diet.
  5. # Cotter DG et al. (2011) Obligate role for ketone body oxidation in neonatal metabolic homeostasis.
  6. # Haninger NC et al. (2001) Screening for hypoglycemia in healthy term neonates: effects on breastfeeding
  7. # Hawdon JM (1999) Hypoglycaemia and the neonatal brain.
  8. # Jain A et al. (2010) Hypoglycemia in the newborn.
  9. # Eidelman AI (2001) Hypoglycemia and the breastfed neonate
  10. # Gartner LM (2001) Breastfeeding and jaundice
  11. # Panburana J et al. (2010) Accuracy of transcutaneous bilirubinometry compare to total serum bilirubin measurement.